Do glia drive synaptic and cognitive impairment in disease?

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Synaptic dysfunction is a hallmark of many neurodegenerative and psychiatric brain disorders, yet we know little about the mechanisms that underlie synaptic vulnerability. Although neuroinflammation and reactive gliosis are prominent in virtually every CNS disease, glia are largely viewed as passive responders to neuronal damage rather than drivers of synaptic dysfunction. This perspective is changing with the growing realization that glia actively signal with neurons and influence synaptic development, transmission and plasticity through an array of secreted and contact-dependent signals. We propose that disruptions in neuron-glia signaling contribute to synaptic and cognitive impairment in disease. Illuminating the mechanisms by which glia influence synapse function may lead to the development of new therapies and biomarkers for synaptic dysfunction.
Publisher
NATURE PUBLISHING GROUP
Issue Date
2015-11
Language
English
Article Type
Article
Keywords

ASTROCYTE-SECRETED PROTEINS; GLUTAMATE TRANSPORTER GLT-1; ALZHEIMERS-DISEASE; MOUSE MODELS; CNS SYNAPTOGENESIS; COMPLEMENT ACTIVATION; EXCITATORY SYNAPSES; MICROGLIAL RESPONSE; TREM2; MICE

Citation

NATURE NEUROSCIENCE, v.18, no.11, pp.1539 - 1545

ISSN
1097-6256
DOI
10.1038/nn.4142
URI
http://hdl.handle.net/10203/206026
Appears in Collection
BS-Journal Papers(저널논문)
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